POS0052 ANGIOGENIC T CELLS AS RELEVANT PLAYERS IN THE LUNG VASCULOPATHY OF RHEUMATOID ARTHRITIS, SYSTEMIC SCLEROSIS AND OTHER AUTOIMMUNE DISEASES
Authors: V. Pulito-Cueto, S. Remuzgo-Martínez, F. Genre, B. Atienza-Mateo, V. Portilla, V. M. Mora-Cuesta, D. Iturbe Fernández, L. Lera-Gómez, J. Rodriguez Carrio, D. Prieto-Peña, R. Blanco, A. Corrales, O. Gualillo, J. M. Cifrián-Martínez, R. López-Mejías, M. A. González-Gay
Journal: Annals of the Rheumatic Diseases (2022)

Background Interstitial lung disease (ILD) is a common and life-threatening complication in patients with autoimmune diseases (AD), mainly in those with systemic sclerosis (SSc) and rheumatoid arthritis (RA). Growing evidence indicate that vascular abnormalities constitute the early phase in the pathogenesis of these inflammatory diseases [1]. We recently reported a decrease of angiogenic T cells (TAng), that promote endothelial repair and revascularization cooperating with endothelial progenitor cells (EPC) [2], in patients with AD-ILD + [3]. Nevertheless, no studies have been conducted on the role of TAng in the presence of ILD in RA, SSc or other AD. Objectives To determine the contribution of TAng in the pathogenic processes of vasculopathy and lung fibrosis in RA-ILD + , SSc-ILD + and other AD-ILD + , as well as their relationship with EPC in all the AD-ILD + patients. Methods Peripheral venous blood was collected from 21 RA-ILD + patients, 21 SSc-ILD + patients and 15 patients with other AD-ILD + . Furthermore, we included 4 comparative groups: 25 RA-ILD - patients, 20 SSc-ILD - patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 21 healthy controls (HC). TAng were considered as CD3 + CD184 + CD31 + cells by flow cytometry. Additionally, EPC data were previously published by Pulito-Cueto et al. [4-5]. Results Regarding the role of TAng in vasculopathy, the frequencies of these cells were significantly lower in patients with RA-ILD + , SSc-ILD + and other AD-ILD + , as well as with IPF in relation to HC (p=0.007, p=0.016, p=0.005 and p&lt;0,001, respectively, Figure 1). No differences between RA-ILD - patients, SSc-ILD - patients and HC were found (Figure 1). With respect to TAng involvement in fibrosis, TAng frequencies were similar in patients with RA-ILD + , SSc-ILD + , other AD-ILD + and those with IPF (Figure 1). Nevertheless, patients with RA-ILD + and SSc-ILD + showed significantly lower TAng frequencies than those with RA-ILD - and SSc-ILD - , respectively (p=0.006 and p=0.044, respectively, Figure 1). In this line, a higher frequency of TAng was found in SSc-ILD - and RA-ILD - patients in relation with those with IPF (p&lt;0.001 and p=0.003, respectively, Figure 1). Moreover, TAng frequency did not show significant correlation with EPC frequency in the whole cohort of AD-ILD + patients. Figure 1. Quantification of TAng population by flow cytometry in all individuals included in the study. Conclusion TAng play a relevant role in the lung vasculopathy of RA-ILD + , SSc-ILD + and other AD-ILD + . Interestingly, circulating TAng may be considered as a useful biomarker of the presence of ILD in patients with RA and SSc. References [1]Expert Rev Clin Immunol 2018;14(1):69-82. [2]Rheum Dis 2015;74(5):921–927. [3]Ann Rheum Dis 2021;80(1):1047-1048. [4]J Clin Med 2020;9(12):4098. [5]Biomedicines 2021;9(7):847. Acknowledgements VP-C is supported by a pre-doctoral grant from IDIVAL (PREVAL18/01); SR-M is supported by funds of the RETICS Program (RD16/0012/0009) from `Instituto de Salud Carlos III´ (ISCIII), co-funded by the European Regional Development Fund; RL-M is a recipient of a Miguel Servet type I programme fellowship from ISCIII, co-funded by the European Social Fund, `Investing in your future’(grant CP16/00033). Disclosure of Interests Verónica Pulito-Cueto: None declared, Sara Remuzgo-Martínez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Virginia Portilla: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe Fernández: None declared, Leticia Lera-Gómez: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Oreste Gualillo: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Abbvie, Pfizer, Roche, Sanofi, Lilly, Celgene, MSD, GSK, Grant/research support from: Abbvie, MSD, Janssen, Roche